Abstract
BackgroundTo investigate the effects of lead exposure and IGF1R inhibitor AG1024 on the expression of IGF1R and IGFBP3 in PC12 cells. It is clear that the mechanism of the related proteins inducing AD is regulated by them, thus providing theoretical guidance for the prevention and treatment of lead poisoning. MethodsThis study is mainly used PC12 neuron cell to cultivate and establish a corresponding lead exposure model, deal with cells with different concentrations of lead acetate respectively, divide the experiment into control group, 1 μmoL/L PbAc, 10 μmoL/L PbAc group, IGF1R inhibitor (AG1024) group, IGF1R inhibitor group (AG1024) + 1 μmoL/L PbAc group, IGF1R inhibitor group (AG1024) + 10 μmoL/L PbAc group, respective contamination’s three periods of time 24 h, 48 h, and 72 h. Lead exposure dose on cell proliferation was examined by MTT. The protein expression of IGF1R and IGFBP3 in PC12 cells were tested by western blotting and immunohistochemistry, The expression of Aβ40 and Aβ42 in cell supernatant was determined by ELISA. ResultsCompared with the control group, the proliferation of the cells in the high-dose lead-exposed group was significantly inhibited (P < 0.05), and the expression of IGF1R and IGFBP3 was significantly decreased (P < 0.05); the contents of Aβ40 and Aβ42 were not statistically significant among the groups (P > 0.05). ConclusionThis study shows that lead can obviously down-regulate the expression of IGF1R and IGFBP3, lead and inhibitor can inhibit the proliferation of cells, promote the tendency of apoptosis, and damage the nervous system.
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